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July 23, 2025Current Enzyme Inhibition0 citations

Dipeptidyl Peptidase-4 – A Comprehensive Review

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VPV. ParthasarathiKHK. Hemalatha

Key Points

  • Dipeptidyl peptidase-4 (DPP-4) is pivotal in managing type 2 diabetes by regulating insulin levels.
  • Inhibiting DPP-4 helps maintain glucose-dependent insulinotropic peptide and glucagon-like peptide 1.
  • The review discusses DPP-4's effects on pancreatic beta cell and skeletal muscle function.
  • Understanding DPP-4 inhibition could lead to new antidiabetic compounds for type 2 diabetes treatment.

Abstract

Abstract: Type 2 diabetes mellitus is a growing global public health issue, with its prevalence projected to increase in the coming decades. It is one of the most prevalent and growing global health concerns, affecting millions of individuals worldwide. The condition is classified into two primary types: Type 1 diabetes, an autoimmune disorder that leads to the destruction of insulin-producing beta cells in the pancreas, and Type 2 diabetes, which is predominantly associated with insulin resistance and inadequate insulin secretion. The various enzymes play a crucial role in the regulation of metabolic pathways, and their dysfunction can contribute to various diseases, including diabetes mellitus. Among these enzymes, the dipeptidyl peptidase-4 serves as a therapeutic target for managing T2D. Inhibiting DPP-4 prevents the breakdown of glucose-dependent insulinotropic peptide and glucagon-like peptide 1, thereby maintaining their natural levels and helping to reduce blood glucose. This review provides a comprehensive overview of the DPP-4 enzyme, including the effects of DPP-4 inhibition on pancreatic beta cell function, skeletal muscle function, and glucose-lowering mechanisms. We believe that this information will aid scientists in developing novel antidiabetic compounds for T2D treatment.

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Cite This Study

Parthasarathi et al. (2025) studied this question.

synapsesocial.com/papers/689a0621e6551bb0af8cdd42https://doi.org/10.2174/0115734080377297250711143404
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